Juvenile hemochromatosis is an iron overload condition caused by mutations in hemojuvelin, which Babitt et al. believe is a cofactor for these proteins. Inhibition of the Wnt signaling pathway by one factor antagonizes the action of these proteins; that aforementioned factor binds to LRP5/6 receptors and is called sclerostin. The expression of fibroblast growth factors and sonic hedgehog require the inhibition of these compounds by gremlin-1. The tenth of these is thought to facilitate heart tabeculation, and the seventh of these triggers SMAD phosphorylation. A metalloprotease in this group cleaves laminin five and three procollagen forms. Noggin and chordin maintain fetus polarity by inhibiting the fourth one of these, which, like many ot
Juvenile hemochromatosis is an iron overload condition caused by mutations in hemojuvelin, which Babitt et al. believe is a cofactor for these proteins. Inhibition of the Wnt signaling pathway by one factor antagonizes the action of these proteins; that aforementioned factor binds to LRP5/6 receptors and is called sclerostin. The expression of fibroblast growth factors and sonic hedgehog require the inhibition of these compounds by gremlin-1. The tenth of these is thought to facilitate heart tabeculation, and the seventh of these triggers SMAD phosphorylation. A metalloprotease in this group cleaves laminin five and three procollagen forms. Noggin and chordin maintain fetus polarity by inhibiting the fourth one of these, which, like many others, is a TGF-beta family protein. For 10 points, name these proteins that can induce new bone to form.
Juvenile hemochromatosis is an iron overload condition caused by mutations in hemojuvelin, which Babitt et al. believe is a cofactor for these proteins.
bone {morphogenic} protein